Work in progress is concerned with the role of potassium deficits in augmenting renal acid excretion during chronic H2SO4 feeding in the dog. The factors responsible for increasing renal acid excretion during mineral acid feeding remain unclear. Recent studies from this laboratory have cast considerable doubt on the classic view that changes in systemic pH mediated the renal response to large acid loads. Because large sodium losses typically develop before full augmentation of renal acid excretion occurs in this model of chronic metabolic acidosis, we recently examined the possibility that an augmented stimulus to sodium reabsorption might play a key role. Experimental evidence, however, did not support this contention. We are presently exploring the alternative possibility that the large potassium deficits that also accumulate before the full augmentation of renal acid excretion occurs might provide a crucial physiologic link between acid feeding and the appropriate renal response. Full metabolic balance studies are being done on animals given large dietary supplements of sulfuric acid before and after the development of potassium deficits.